Role of radiation in human leukemia

In the analysis of radiation induced leukemia only two studies (one on the survivors of the atomic bombing and the other the British series on ankylosing spondylitics) appear to show a causal relationship. In both studies, a peak in the occurrence of leukemia was reached about five years from the initial exposure: The dose-response curves were approximately linear between 50-450 rads (A-bomb survivors) and 300-1,500 rads (spondylitics), and their excess in leukemia incidence was about 1-2 cases/106/year/rad. The cancer incidence of A-bomb survivors has shown that after a latency period of two or three years the number of cases of leukemias increased rapidly to peak in 1950-1952. During this period, leukemia deaths were more than 50 times normal in the highest dose group and by 1965-1970 were about eight times normal. For other cancers, by 1965-1970, deaths were about one and one-half times normal, i.e., an increase of about 50 percent among the survivors who had doses exceeding 100 rads. In ankylosing spondylitic patients treated with x-rays, certain trends were observed. In utero exposure to A-bomb irradiation involves five studies: Childhood cancer, sex rations, mortality, growth and development, and mental retardation. No increase in the incidence rate of solid tumors and leukemia was observed during the first ten years after the bombings. The findings from the study of in utero exposure to clinical x-rays, radiation exposure to radiologists, and therapeutic irradiation to the pelvic region were all inconclusive. Although a common etiology for leukemia goes unidentified, evidence now available suggests that the mechanism of leukemogenesis in man involves a block or an aberration in one or more factors associated with white cell maturation. A proposed sequence of events involving major potential leukemogenic factors such as radiation, viral, chemical, genetic, and hormonal factors is presented